{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n BZRAP1‐AS1 is a long noncoding RNA whose dysregulation appears to contribute to the pathogenesis of several human diseases through effects on cell proliferation, inflammation, and angiogenesis. In hepatocellular carcinoma, BZRAP1‐AS1 is highly expressed and promotes angiogenesis by binding to DNA methyltransferase 3B (DNMT3b) to induce methylation of the thrombospondin‐1 (THBS1) promoter, thereby reducing THBS1 transcription and enhancing endothelial cell proliferation, migration, and tube formation (1). In rheumatoid arthritis, BZRAP1‐AS1 is downregulated in affected synoviocytes, and its overexpression counteracts disease progression by sequestering miR‐1286. This “sponging” effect leads to the upregulation of COL5A2, which in turn suppresses pathological cell proliferation and inflammatory cytokine production while promoting apoptosis (2). In prostate cancer, BZRAP1‐AS1 has been identified as a key node in transcriptional regulatory networks, suggesting that its altered expression may serve as a novel biomarker and contribute to disease pathogenesis (3). Moreover, genetic variants within the BZRAP1‐AS1 locus have been linked to Alzheimer’s disease pathology, indicating that it could also participate in the modulation of inflammatory and hematological phenotypes associated with neurodegeneration (4). Finally, BZRAP1‐AS1 has emerged from co‐expression and competing endogenous RNA analyses as a differentially expressed hub molecule in both acute myocardial infarction and pediatric acute lymphoblastic leukemia, hinting at a broader involvement in immune regulation and cellular stress responses (5,6).\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n (1)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "; (2)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "; (3)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": "; (4)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": "; (5)"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": "; (6)."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Weiwei Wang, Guoyong Chen, Bing Wang, et al. 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